In 1921, Rollin Turner Woodyatt reviewed the research on diet and diabetes. He reported that three water-soluble compounds, β-hydroxybutyrate, acetoacetate, and acetone (known collectively as ketone bodies), were produced by the liver in otherwise healthy people when they were starved or if they consumed a very low-carbohydrate, high-fat diet. Dr. Russell Morse Wilder, at the Mayo Clinic, built on this research and coined the term "ketogenic diet" to describe a diet that produced a high level of ketone bodies in the blood (ketonemia) through an excess of fat and lack of carbohydrate. Wilder hoped to obtain the benefits of fasting in a dietary therapy that could be maintained indefinitely. His trial on a few epilepsy patients in 1921 was the first use of the ketogenic diet as a treatment for epilepsy.
Variations on the Johns Hopkins protocol are common. The initiation can be performed using outpatient clinics rather than requiring a stay in hospital. Often, no initial fast is used (fasting increases the risk of acidosis, hypoglycaemia, and weight loss). Rather than increasing meal sizes over the three-day initiation, some institutions maintain meal size, but alter the ketogenic ratio from 2:1 to 4:1.
If you want to lose weight, avoid special “low-carb” products that are full of carbs. This should be obvious, but creative marketers are doing all they can to fool you (and get your money). They will tell you that you can eat cookies, pasta, ice cream, bread and plenty of chocolate on a low-carb diet, as long as you buy their brand. They’re often full of carbohydrates. Don’t be fooled.
Young males sometimes lose weight faster than this, perhaps twice as fast. Post-menopausal women may lose at a slower pace. People on a very strict low-carb diet may lose weight quicker, as well as those who exercise a lot (a bonus). And if you have an enormous amount of excess weight to lose you could start out much faster — although initially, some of the weight you lose will be due to water loss.
If you have type 2 diabetes there is another diabetes drug that can result in noticeable weight loss: the “low-carb in a pill” drug Farxiga (called Forxiga in Europe). Unfortunately, this pill has an increased risk of ketoacidosis, probably especially for people on strict low-carb or keto diets, and it’s not recommended to take this drug while on a strict low-carb diet.
Physicians of ancient Greece treated diseases, including epilepsy, by altering their patients' diet. An early treatise in the Hippocratic Corpus, On the Sacred Disease, covers the disease; it dates from c. 400 BC. Its author argued against the prevailing view that epilepsy was supernatural in origin and cure, and proposed that dietary therapy had a rational and physical basis.[Note 3] In the same collection, the author of Epidemics describes the case of a man whose epilepsy is cured as quickly as it had appeared, through complete abstinence of food and drink.[Note 4] The royal physician Erasistratus declared, "One inclining to epilepsy should be made to fast without mercy and be put on short rations."[Note 5] Galen believed an "attenuating diet"[Note 6] might afford a cure in mild cases and be helpful in others.
Normal dietary fat contains mostly long-chain triglycerides (LCTs). Medium-chain triglycerides (MCTs) are more ketogenic than LCTs because they generate more ketones per unit of energy when metabolised. Their use allows for a diet with a lower proportion of fat and a greater proportion of protein and carbohydrate, leading to more food choices and larger portion sizes. The original MCT diet developed by Peter Huttenlocher in the 1970s derived 60% of its calories from MCT oil. Consuming that quantity of MCT oil caused abdominal cramps, diarrhea, and vomiting in some children. A figure of 45% is regarded as a balance between achieving good ketosis and minimising gastrointestinal complaints. The classical and modified MCT ketogenic diets are equally effective and differences in tolerability are not statistically significant. The MCT diet is less popular in the United States; MCT oil is more expensive than other dietary fats and is not covered by insurance companies.
This might be because the body increases insulin secretion in anticipation that sugar will appear in the blood. When this doesn’t happen, blood sugar drops and hunger increases. Whether this chain of events regularly takes place is unclear. Something odd happened when I tested Pepsi Max though, and there are well-designed studies showing increased insulin response when using artificial sweeteners.
The ketogenic diet is usually initiated in combination with the patient's existing anticonvulsant regimen, though patients may be weaned off anticonvulsants if the diet is successful. Some evidence of synergistic benefits is seen when the diet is combined with the vagus nerve stimulator or with the drug zonisamide, and that the diet may be less successful in children receiving phenobarbital.
If you’re looking to get a jump start on your health and fitness goals this year, you may be thinking about trying the ketogenic diet. Maybe you’ve heard the phrase before — it’s a huge diet buzzword — but aren’t sure what it means. Here’s a primer: The ketogenic diet is an eating plan that drives your body into ketosis, a state where the body uses fat as a primary fuel source (instead of carbohydrates), says Stacey Mattinson, RDN, who is based in Austin, Texas.
When in the hospital, glucose levels are checked several times daily and the patient is monitored for signs of symptomatic ketosis (which can be treated with a small quantity of orange juice). Lack of energy and lethargy are common, but disappear within two weeks. The parents attend classes over the first three full days, which cover nutrition, managing the diet, preparing meals, avoiding sugar, and handling illness. The level of parental education and commitment required is higher than with medication.
After initiation, the child regularly visits the hospital outpatient clinic where they are seen by the dietitian and neurologist, and various tests and examinations are performed. These are held every three months for the first year and then every six months thereafter. Infants under one year old are seen more frequently, with the initial visit held after just two to four weeks. A period of minor adjustments is necessary to ensure consistent ketosis is maintained and to better adapt the meal plans to the patient. This fine-tuning is typically done over the telephone with the hospital dietitian and includes changing the number of calories, altering the ketogenic ratio, or adding some MCT or coconut oils to a classic diet. Urinary ketone levels are checked daily to detect whether ketosis has been achieved and to confirm that the patient is following the diet, though the level of ketones does not correlate with an anticonvulsant effect. This is performed using ketone test strips containing nitroprusside, which change colour from buff-pink to maroon in the presence of acetoacetate (one of the three ketone bodies).
On the ketogenic diet, carbohydrates are restricted and so cannot provide for all the metabolic needs of the body. Instead, fatty acids are used as the major source of fuel. These are used through fatty-acid oxidation in the cell's mitochondria (the energy-producing parts of the cell). Humans can convert some amino acids into glucose by a process called gluconeogenesis, but cannot do this by using fatty acids. Since amino acids are needed to make proteins, which are essential for growth and repair of body tissues, these cannot be used only to produce glucose. This could pose a problem for the brain, since it is normally fuelled solely by glucose, and most fatty acids do not cross the blood–brain barrier. However, the liver can use long-chain fatty acids to synthesise the three ketone bodies β-hydroxybutyrate, acetoacetate and acetone. These ketone bodies enter the brain and partially substitute for blood glucose as a source of energy.
In so far as insulin promotes de novo lipogenesis and suppresses lipolysis in adipocytes it DOES help keep the fat inside. But in Hyperinsulinemia / Insulin Resistance with Impaired Glucose Tolerance lipolysis may not be sufficiently reduced and fatty acids and glycerin can be spilled at the same time that Triglycerides are being formed & stored. In the liver the glycerin gets converted to glucose producing hyperglycemia.
Early studies reported high success rates; in one study in 1925, 60% of patients became seizure-free, and another 35% of patients had a 50% reduction in seizure frequency. These studies generally examined a cohort of patients recently treated by the physician (a retrospective study) and selected patients who had successfully maintained the dietary restrictions. However, these studies are difficult to compare to modern trials. One reason is that these older trials suffered from selection bias, as they excluded patients who were unable to start or maintain the diet and thereby selected from patients who would generate better results. In an attempt to control for this bias, modern study design prefers a prospective cohort (the patients in the study are chosen before therapy begins) in which the results are presented for all patients regardless of whether they started or completed the treatment (known as intent-to-treat analysis).
The brain is composed of a network of neurons that transmit signals by propagating nerve impulses. The propagation of this impulse from one neuron to another is typically controlled by neurotransmitters, though there are also electrical pathways between some neurons. Neurotransmitters can inhibit impulse firing (primarily done by γ-aminobutyric acid, or GABA) or they can excite the neuron into firing (primarily done by glutamate). A neuron that releases inhibitory neurotransmitters from its terminals is called an inhibitory neuron, while one that releases excitatory neurotransmitters is an excitatory neuron. When the normal balance between inhibition and excitation is significantly disrupted in all or part of the brain, a seizure can occur. The GABA system is an important target for anticonvulsant drugs, since seizures may be discouraged by increasing GABA synthesis, decreasing its breakdown, or enhancing its effect on neurons.
We’ve now arrived at tip number 16. If you’re still having trouble losing weight, despite following the 15 pieces of advice listed above, it might be a good idea to bring out the heavy artillery: optimal ketosis. Many people stalling at weight plateaus while on a low-carb diet have reported finding optimal ketosis helpful. It’s what can melt the fat off once again.
Work indulgence foods into your calorie plan. If you do want to have something that is a little higher in calories, then make sure that you work it into your overall calorie goal for the day. For example, if you are following a 1,800 calorie plan, and you want to have a brownie that is 300 calories, then you would only have 1,500 calories left for the day.
This drug is an injected variant of a satiety hormone called GLP-1. It slows down how quickly the stomach empties and tells the brain that you don’t need to eat yet – not a bad idea for losing weight. As a bonus this drug works fine while one is on the keto diet and it works even better with intermittent fasting – for a rapid weight loss with no hunger.
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